Rhein Relieves Oxidative Stress in an Aβ_1-42 Oligomer-Burdened Neuron Model by Activating the SIRT1/PGC-1α-Regulated Mitochondrial Biogenesis.

ABSTRACT: Neuronal mitochondrial oxidative stress induced by β-amyloid (Aβ) is an early event of Alzheimer's disease (AD). Emerging evidence has shown that antioxidant therapy represents a promising therapeutic strategy for the treatment of AD. In this study, we investigated the antioxidant activity of rhein against Aβ_1-42 oligomer-induced mitochondrial oxidative stress in primary neurons and proposed a potential antioxidant pathway involved. The results suggested that rhein significantly reduced reactive oxygen species (ROS) level, reversed the depletion of mitochondrial membrane potential, and protected neurons from oxidative stress-associated apoptosis. Moreover, further study indicated that rhein activated mitochondrial biogenesis accompanied by increased cytochrome C oxidase (CytOx)

SUBMITTER: Yin Z 

PROVIDER: S-EPMC8461019 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature